醇通过调节细胞核中的MAPK通路来减少IL-1β诱导的亡和退化
Chao Yu1, Xiaodong Wei1, Jiaxi Wang2
1The Second Department of Spine Surgery, Yantaishan Hospital, Yantai, 264003, Shandong, China.
Biochemical and biophysical research communications
|September 26, 2025
概括
帕埃诺尔通过减少细胞亡,炎症和细胞外基质降解来防止椎间盘退化 (IDD). 它通过抑制基因激活蛋白激酶 (MAPK) 信号通路来实现这一目标.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 椎间盘退化 (IDD) 是一种衰弱的疾病,其特征是细胞衰老,细胞亡,炎症和细胞外基质 (ECM) 退化.
- 了解IDD背后的分子机制对于开发有效的治疗策略至关重要.
研究的目的:
- 为了研究醇对IDD的治疗作用.
- 阐明IDD中帕埃诺的基础调节机制,重点关注基因激活蛋白激酶 (MAPK) 信号通路.
主要方法:
- 一个细胞模型的IDD是建立使用人细胞核脉 (NP) 细胞治疗白蛋白-1β (IL-1β).
- 细胞活力,衰老和细胞亡被评估使用细胞计数套件-8试验,β-galactosidase染色和流细胞计.
- 与衰老,亡,炎症,ECM降解和MAPK途径相关的基因和蛋白质表达水平使用RT-qPCR,西斑和免疫光染色进行了分析.
- 网络药理学分析被用来探索醇的分子机制.
主要成果:
- 在IDD模型中,Paeonol治疗显著增强了NP细胞活力,抑制了衰老和亡,减轻了炎症和ECM降解.
- 醇降低了衰老标记物 (p16INK4a),与亡相关的蛋白质 (Bax,裂开的卡斯帕酶-3),炎症调解物 (IL-6, iNOS, COX-2) 和ECM降解酶 (MMP13, ADAMTS5) 的表达,同时增加了原II水平.
- 网络药理学发现了 paeonol 和 MAPK 信号通路,特别是 MAPK14 (p38) 之间的联系. 醇降低了p38和酸化p38 (p-p38) 的水平.
- 过度表达p38逆转了paeonol对NP细胞活力,细胞亡,炎症和ECM降解的保护作用.
结论:
- 醇通过减轻NP细胞亡,炎症和ECM降解来证明对IDD的保护作用.
- 醇的治疗机制涉及抑制MAPK信号通路.
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